Matches in SemOpenAlex for { <https://semopenalex.org/work/W175265556> ?p ?o ?g. }
Showing items 1 to 77 of
77
with 100 items per page.
- W175265556 abstract "Diversity in plant architecture is largely generated by the post-embryonic regulation of meristem initiation and activity. In a phenomenon known as apical dominance, the active growth of the shoot apical meristem (SAM) exerts significant inhibitory force on the outgrowth of axillary meristems (AMs) into shoot branches. The degree of branching in plants is a determinant of yield in many crop species and is carefully regulated to ensure that plants only branch at specific stages of development or in response to their environment. Apical dominance has been attributed to the action of the hormone auxin, produced in SAM tissues and transported downwards. A second hormone, cytokinin, acts antagonistically to auxin to promote branching. Nonetheless, the exact mechanism by which these hormones operate is still being elucidated and continued research suggested that novel signals are involved. The recent discovery that strigolactones, previously implicated in parasitic weed germination and mycorrhizal associations, are branching inhibitors supports the existence of additional signals controlling branching in plants. In garden pea (Pisum sativum) strigolactones are synthesised by the coordinated action of the carotenoid cleavage dioxygenase (CCD) family enzymes, RMS1 (RAMOSUS1) and RMS5. These are encoded by MAX4 (MORE AXILLARY GROWTH4) and MAX3 in Arabidopsis thaliana respectively. Mutants for MAX genes have increased amounts of auxin travelling in the polar auxin transport stream (PATS) of inflorescence stems but exhibit increased branching that is insensitive to inhibition by this auxin. Two hypotheses for the action of strigolactones have been presented. The first is that strigolactones modulate the levels of auxin transport proteins, preventing axillary buds from establishing an active auxin transport flow into the primary stem, which inhibits growth. The second is that strigolactones act downstream of auxin signalling to inhibit the action of outgrowth-promoters. Consistent with this latter hypothesis, in pea, rice (Oryza sativa) and petunia (Petunia hybrida), the expression of RMS1/MAX4 orthologues is auxin regulated. These genes are also regulated by feedback signalling in strigolactone pathway mutants and this is proposed to involve an additional novel signal. In Arabidopsis, however, research showed that MAX4 is not regulated by feedback or auxin in the shoot and placed doubt on the importance of this regulation for branching control. The strigolactone biosynthetic pathway offers a novel target for the manipulation of plant architecture and yield while controlling the germination of parasitic weed species that are detrimental to agriculture. Therefore, a greater understanding of the pathway and its regulators is beneficial. The majority of the research in this thesis pre-dates the discovery of strigolactones as the RMS/MAX-derived branching inhibitor, yet aimed to clarify the evolutionary conservation and functional importance of the regulation of strigolactone biosynthetic genes by auxin and feedback signalling in Arabidopsis. Quantitative real-time PCR analysis demonstrated that MAX3 and MAX4 are co-ordinately and systemically regulated by auxin and by feedback throughout development. Both auxin and feedback regulation required the AXR1/TIR1 auxin response pathway, which targets Aux/IAA transcriptional repressors for proteasomal degradation. In particular, correct degradation of the Aux/IAA protein IAA12 appears to be necessary for optimal MAX3 and MAX4 expression. Moreover this regulation affects strigolactone-dependent branching inhibition. Therefore it is proposed that auxin inhibits branching, in part, by positively regulating strigolactone synthesis. As feedback requires AXR1, this also suggests that increased auxin level and/or signalling in the PATS in conditions of reduced strigolactone signalling mediates feedback regulation of the strigolactone pathway. Consistent with this, microarray analysis revealed that in addition to the inflorescence, max mutants have increased global auxin-responsive gene expression associated with the PATS in the vegetative stage. The pea RMS1 gene was the first strigolactone pathway gene demonstrated to be auxin-regulated. Sequencing of the RMS1 promoter and comparative bioinformatic analysis with promoters of other strigolactone synthesis genes revealed a number of conserved, putative regulatory cis-elements that could mediate this regulation and cross-talk with additional branching cues. However a 2.5 kb fragment of the RMS1 promoter was not sufficient to drive transcriptional and translational fusions with GFP and the RMS1 coding region in Arabidopsis. The RMS1 coding region driven by the CAMV 35S promoter complemented the max4 mutant but did not affect branching induced by auxin-depleting treatments. Grafting studies with axr1 and iaa12 mutants, and decapitation and auxin-transport inhibition in max4 mutants, demonstrated that auxin signalling has a function in branching control independent from the regulation of strigolactone synthesis genes. Overall, data obtained herein was incorporated into current models for the interaction of the strigolactone pathway with auxin and cytokinin in the control of shoot branching. It is suggested that both strigolactone and auxin have the capacity to regulate the levels or distribution of each other in interlocking feedback loop that intersects with additional developmental, physiological and environmental cues for the precise control of axillary branching in plants." @default.
- W175265556 created "2016-06-24" @default.
- W175265556 creator A5081688498 @default.
- W175265556 date "2009-04-01" @default.
- W175265556 modified "2023-09-27" @default.
- W175265556 title "Interactions between auxin and strigolactone in the control of arabidopsis shoot branching" @default.
- W175265556 hasPublicationYear "2009" @default.
- W175265556 type Work @default.
- W175265556 sameAs 175265556 @default.
- W175265556 citedByCount "0" @default.
- W175265556 crossrefType "journal-article" @default.
- W175265556 hasAuthorship W175265556A5081688498 @default.
- W175265556 hasConcept C104317684 @default.
- W175265556 hasConcept C126021549 @default.
- W175265556 hasConcept C143065580 @default.
- W175265556 hasConcept C178165689 @default.
- W175265556 hasConcept C202751555 @default.
- W175265556 hasConcept C207778908 @default.
- W175265556 hasConcept C21410773 @default.
- W175265556 hasConcept C2776822380 @default.
- W175265556 hasConcept C2778177256 @default.
- W175265556 hasConcept C2779491563 @default.
- W175265556 hasConcept C2780369116 @default.
- W175265556 hasConcept C2780813515 @default.
- W175265556 hasConcept C37351400 @default.
- W175265556 hasConcept C55493867 @default.
- W175265556 hasConcept C55580049 @default.
- W175265556 hasConcept C59822182 @default.
- W175265556 hasConcept C86803240 @default.
- W175265556 hasConcept C90703135 @default.
- W175265556 hasConcept C95444343 @default.
- W175265556 hasConceptScore W175265556C104317684 @default.
- W175265556 hasConceptScore W175265556C126021549 @default.
- W175265556 hasConceptScore W175265556C143065580 @default.
- W175265556 hasConceptScore W175265556C178165689 @default.
- W175265556 hasConceptScore W175265556C202751555 @default.
- W175265556 hasConceptScore W175265556C207778908 @default.
- W175265556 hasConceptScore W175265556C21410773 @default.
- W175265556 hasConceptScore W175265556C2776822380 @default.
- W175265556 hasConceptScore W175265556C2778177256 @default.
- W175265556 hasConceptScore W175265556C2779491563 @default.
- W175265556 hasConceptScore W175265556C2780369116 @default.
- W175265556 hasConceptScore W175265556C2780813515 @default.
- W175265556 hasConceptScore W175265556C37351400 @default.
- W175265556 hasConceptScore W175265556C55493867 @default.
- W175265556 hasConceptScore W175265556C55580049 @default.
- W175265556 hasConceptScore W175265556C59822182 @default.
- W175265556 hasConceptScore W175265556C86803240 @default.
- W175265556 hasConceptScore W175265556C90703135 @default.
- W175265556 hasConceptScore W175265556C95444343 @default.
- W175265556 hasLocation W1752655561 @default.
- W175265556 hasOpenAccess W175265556 @default.
- W175265556 hasPrimaryLocation W1752655561 @default.
- W175265556 hasRelatedWork W1980141674 @default.
- W175265556 hasRelatedWork W1999717088 @default.
- W175265556 hasRelatedWork W2007526647 @default.
- W175265556 hasRelatedWork W2038821251 @default.
- W175265556 hasRelatedWork W2074005430 @default.
- W175265556 hasRelatedWork W2091717318 @default.
- W175265556 hasRelatedWork W2098382831 @default.
- W175265556 hasRelatedWork W2125524099 @default.
- W175265556 hasRelatedWork W2125953732 @default.
- W175265556 hasRelatedWork W2127986909 @default.
- W175265556 hasRelatedWork W2136196281 @default.
- W175265556 hasRelatedWork W2139632133 @default.
- W175265556 hasRelatedWork W2162277706 @default.
- W175265556 hasRelatedWork W2163260369 @default.
- W175265556 hasRelatedWork W2168203902 @default.
- W175265556 hasRelatedWork W2475796852 @default.
- W175265556 hasRelatedWork W2921737581 @default.
- W175265556 hasRelatedWork W2968106159 @default.
- W175265556 hasRelatedWork W2442465912 @default.
- W175265556 hasRelatedWork W2500667092 @default.
- W175265556 isParatext "false" @default.
- W175265556 isRetracted "false" @default.
- W175265556 magId "175265556" @default.
- W175265556 workType "article" @default.